Delayed contrast enhancement and perfusable tissue index in hypertrophic cardiomyopathy: Comparison between cardiac MRI and PET

Paul Knaapen*, Willem G. Van Dockum, Olga Bondarenko, W. E M Kok, M. J W Götte, Ronald Boellaard, Aernout M. Beek, Cees A. Visser, Albert C. Van Rossum, Adriaan A. Lammertsma, Frans C. Visser

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Delayed contrast enhancement (DCE) visualized by cardiac MRI (CMR) is a common feature in patients with hypertrophic cardiomyopathy (HCM), presumed to be related to myocardial fibrosis. The pathophysiologic basis of hyperenhancement in this patient group, however, remains unclear as limited histologic comparisons are available. The present study compares the perfusable tissue index (PTI), an alternative marker of myocardial fibrosis obtained by PET, with DCE-CMR in HCM. Methods: Twenty-one patients with asymmetric septal HCM, 12 chronic myocardial infarction (MI) patients, and 6 age-matched healthy control subjects were studied with DCE-CMR and PET. PET was performed using 15O-labeled water and carbon monoxide to obtain the PTI. Results: No hyperenhancement was observed in control subjects and the PTI was within normal limits (1.10 ± 0.07 [mean ± SD]). In MI patients, the extent of hyperenhancement (25% ± 16% [mean ± SD]) was inversely related to the decrease in the PTI (0.94 ± 0.12; r = -0.65, P < 0.05). Average hyperenhancement in HCM was 14% ± 12%, predominantly located in the interventricular septum. The PTI in the hypertrophied interventricular septum, however, was not reduced (1.12 ± 0.13). Furthermore, in contrast to MI patients, there was a modest positive correlation between the extent of DCE and the PTI in HCM (r = 0.45, P < 0.05). Conclusion: DCE in the hypertrophied septum of HCM patients is not accompanied by a decline in the PTI, and there is a positive correlation between the extent of DCE and the PTI. These results suggest that hyperenhancement may not be caused solely by fibrotic replacement scarring in this patient group. Other pathologic changes associated with HCM may also cause gadolinium-diethylenetriaminepentaacetic acid hyperenhancement.

Original languageEnglish
Pages (from-to)923-929
Number of pages7
JournalJournal of Nuclear Medicine
Issue number6
Publication statusPublished - 1 Dec 2005

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